Talk:Psilocin

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Ideal sources for Wikipedia's health content are defined in the guideline Wikipedia:Identifying reliable sources (medicine) and are typically review articles. Here are links to possibly useful sources of information about Psilocin.

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Other potential sources include: Centre for Reviews and Dissemination and CDC

My personal belief[edit]

Manna is teonanactl, they are one and the same. I view serotonin to be more of a hallucinogen than psilocin, because with serotonin one is tricked into believing that the world is a much simpler place than it really is ;) Seek manna, God Bless.

This is a simplistic understanding of the serotonin system. Serotonin receptors' primary roles in the body are not psychoactive at all. Serotonin regulates a number of bodily functions, from breathing to smooth muscle contraction in the intestines. Serotonin also remains active at 5HT2a receptors while experiencing a psychedelic; psilocin does not 'replace' serotonin while it's active, it merely shares a receptor site. The only psychoactive experience I can think of that is linked directly to increased serotonin activity is MDMA, a psychedelic in its own right that certainly doesn't "trick [us] into believing that the world is a much simpler place than it really is."

With all due respect, I think it's your ungrounded approach to psychedelic research that makes the world seem like a simpler place than it really is. Psilocin isn't some magical spirit compound; it's one of hundreds of known distinct 5HT2a partial agonists, each with wonderful and unique effects. By deciding you've learned all there is to learn about this subject without even looking to the empirical evidence, you've done yourself a disservice. Don't confuse science with empirical reductionism; it's perfectly possible to believe psychedelics are an important 'gateway to the soul' with much to teach us as individuals and as a species, while remaining fully grounded in empirical evidence. In fact, it's an amazingly exciting field. Do some reading - the truth is far more weird and wonderful than your simple mythology. —Preceding unsigned comment added by 99.129.135.10 (talk) 22:39, 31 August 2010 (UTC)[reply]

Minor Correction[edit]

Although everyone spells it Psilocin technically there was a movement in the scientific community in the '70s to homoginize the naming structure of thes indoles (which are amines/alkaloid) by having an "e" at the end. I know this really is trivial as it essentially did not work we still spell it without the added "e" but in the science world is should officially be "psilocine" and "psiloybine"... I think we just don't like the way it looks though, I know I don'! (Compare mescaline, dimethyltryptamine these are amine <-- see the e?) I don't know it's all lame names for something much cooler.

"Technically" that movement failed. Look in any reputable medical text that addresses the topic and you'll see psilocin, not psilocine. The common name is of little concern to science, anyway; any serious scientific study into the compound would most likely refer to it by its IUPAC name: 4-Hydroxy-N,N-dimethyl-tryptamine. Anything else is glorified drug slang, really. —Preceding unsigned comment added by 99.129.135.10 (talk) 22:47, 31 August 2010 (UTC)[reply]

neurochemistry?[edit]

Does anyone know the chemical action of psilocin once in the brain? Specifically which parts it affects (stimulation, inactivation, etc.) Sequoyah 07:12, 27 February 2006 (UTC)[reply]

Like every other psychedelic hallucinogen it activates the 5-HT_2A serotonin receptors which are located on pyramidal cells of the cerebral cortex. Certain cortical areals, especially the prefrontal cortex, are stimulated by this mechanism and selective 5-HT_2A antagonists like ketanserin block the effects of hallucinogens in humans. See the studies by Franz X. Vollenweider and search Medline or Google using the keywords provided. Cacycle 16:13, 27 February 2006 (UTC)[reply]

The effects of Salvinorin A and ketamine do not stem from action on the 5-HT_2A receptors. 194.46.227.25 (talk) 13:37, 1 May 2010 (UTC)[reply]

Citation Needed?[edit]

It says that psilocin is an agonist for certain hydroxytryptamine receptors in one part of the article with a citation, but then says citation needed when it says it mimicks serotonin. The first citation covers this, an agonist activates a receptor. It is admittadly a redundant comment added in by someone with a limited understanding though.24.65.42.159 (talk) 22:19, 24 October 2008 (UTC)[reply]

I removed the 'mimics serotonin' comment. It's inaccurate. There are hundreds of selective serotonin agonists that produce psychedelic effects through their activity at 5HT2a, each with distinct effects based on a different pattern of activity at that receptor subset. None of them that I'm aware of do anything I would call 'mimicking' serotonin; this should be obvious simply from comparing the effects of serotonergic stimulation of this receptor to a psychedelic experience. Serotonin reuptake inhibitors and serotonin releasers are both quite well-studies categories of drugs, and the effects of increased levels of serotonin in the brain are not at all analogous to a psychedelic trip. I cleaned up the discussion of MAOIs while I was at it, using their full name (the previous article mentioned monoamine oxidase but never defined the acronym 'MAOI') and retaining the warning that this combination can produce uncomfortably intense effects while removing the false claim that the combination could render psilocin itself dangerous. Physiologically, the only dangerous part of an MAOI+psilocin dose is the MAOI itself. While many recreational drugs can build up to toxic levels if combined in excessive doses with an MAOI, psilocin is not one of them. —Preceding unsigned comment added by 99.129.135.10 (talk) 22:45, 31 August 2010 (UTC)[reply]

3d model of psylocin[edit]

Is it just me or doesn't it seem like the 3d model of the psylocin compound doesn't contain or show the hydroxyl group attached to the benzene ring. Did someone mistakenly posted a DMT picture instead of psilocin?--Deus911 17:14, 22 April 2011 (UTC)

Nope, it's not just you. I came to the discussion to point that out as well; no red, no oxygen- it's definitely DMT, not psilocin. What I'm wondering now is, is there a program one can use to make those spinning 3D models? For the sake of correctness, I will answer the question myself.David Baldi (talk) 18:27, 4 May 2011 (UTC)[reply]

Psilocin pharmacology[edit]

Psilocybin is rapidly dephosphorylated in the body to psilocin which acts as a 5-HT2A, 5-HT2C and 5-HT1A agonist or partial agonist. Psilocin exhibits functional selectivity in that it activates phospholipase A2 instead of activating phospholipase C as the endogenous ligand serotonin does.

There is this statement followed by a citation. The citation is a paper on "functional selectivity" and doesn't mention psilocin at all. So this is a wrong citation and I am going to remove it.

This is the paper that was cited: Functional Selectivity and Classical Concepts of Quantitative Pharmacology — Preceding unsigned comment added by 130.226.104.3 (talk) 15:42, 12 January 2017 (UTC)[reply]

psilocybin and clozapine[edit]

I have been using clozapine for several months now (200mg daily), and have learned that it diminishes the psychoactive effect of psilocybin. I have failed to gather data on how long i should cease clozapine in order to have a magic mushrooms trip..? --Namaste@^? 13:52, 24 January 2019 (UTC)[reply]

no signifcant effect on dopamine receptors?[edit]

I've encountered a publication (Ray, 2010) [1] claiming that psilocin binds to D1, D3 more stronger than to 5H_2A, 5HT_2C.

according to this review, [2] it would be like that:

5HT_2B>5HT_1D>D₁>5HT_1E>5HT_1A>5HT_5A>5HT₇>5HT₆>D₃>5HT_2C>5HT_1B>5HT_2A.

can somebody take a look Mekatra (talk) 22:01, 4 April 2023 (UTC)[reply]